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Biomedical subjects

C Tang

Publications and source records attributed to C Tang.

At least 181 records · Page 10Linked to original sources
PubMed1995

Regulation of the ferredoxin component of renal hydroxylases at transcriptional and postranslational levels and of the protein inhibitor of cyclic AMP-dependent kinase.

We have studied two proteins potentially involved in the regulation of the 25-OH-D-1-hydroxylase, which is located in the renal mitochondria and which is responsible for the production of the steroid hormone 1,25(OH)2D3. The endogenous inhibitor of cyclic AMP-dependent protein kinase, PKI, is down regulated by 1,25(OH)2D3. Having cloned and sequenced PKI cDNA, we studied its message levels and found them to be regulated by 1,25(OH)2D3 tissue specifically in the kidney and in kidney cell culture. In other experiments we over expressed the ferredoxin component of the 1-hydroxylase and found it to be physically and chemically indistinguishable from those of classic steroidogenic tissues. The mRNA encoding the ferredoxin component is up-regulated by chronic vitamin D deficiency, which at the same time leads to sustained elevation in 1-hydroxylase activity; no short term effect of 1,25(OH)2D3 on ferredoxin mRNA in kidney cell culture could be demonstrated. Finally, there was an association between decreased phosphorylation of ferredoxin and decreased 1-hydroxylase activity brought about by treatment of cultured kidney cells with TPA. Control of the renal signaling events involved in the production of 1,25(OH)2D3 remains a fruitful area of investigation in the field of the metabolism and actions of vitamin D and its metabolites.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1995

Gut peptide receptors in pancreata of azaserine-treated and normal control rats.

Gut peptides are involved in the growth and carcinogenesis of the exocrine pancreas of rats after treatment with azaserine. However, little is known about the influence of azaserine on expression of gut peptide receptors in the pancreas of the rat. Cholecystokinin, bombesin, somatostatin, secretin, and vasoactive intestinal peptide receptors were therefore visualized and quantified by storage phosphor autoradiography in pancreata of either saline control or azaserine-treated rats. As expected, putative preneoplastic lesions were formed in the pancreata of the azaserine-treated but not in the control animals. The pancreata of control rats contained receptors for cholecystokinin, bombesin, somatostatin, secretin, and vasoactive intestinal peptide. Cholecystokinin receptors were of the A-type and showed, in contrast to the other receptors, a heterogeneous expression due to variability of the high-affinity receptors. In the pancreata of azaserine-treated animals a significantly increased binding capacity of high-affinity receptors fro cholecystokinin was found not only in atypical acinar cell nodules but also in non-nodular pancreas when compared to pancreas of control rats (P < 0.05). Neither atypical acinar cell nodules nor non-nodular pancreas of rats treated by azaserine were shown to possess receptors for the other four types of gut peptide receptors. The spectrum of peptide receptors in pancreas of control and azaserine-treated rats in this study may help to understand the mechanism whereby gut hormones may modulate pancreatic carcinogenesis.

Animals↗
PubMed1995

pIXY321 protects against Ara-C or taxol-induced apoptosis and loss of clonogenic survival of normal human bone marrow progenitor cells.

By suppressing apoptosis, hemopoietic growth factors (HGFs) promote the survival of CD34+, HLA-DR+ marrow cells that are enriched for hemopoietic progenitor cells (HPC). In the present studies, we have examined the effects of pIXY321, a genetically engineered fusion protein of GM-CSF and IL-3 (GM-CSF/IL-3), on high-dose Ara-C (HIDAC) and taxol-induced apoptosis and survival of a multilineage HPC, the CFU-GEMM. Exposure to 1.0 mumol/l taxol for 24 h or HIDAC > or = 10 mumol/l for 4 h induced internucleosomal DNA fragmentation and the morphologic features of apoptosis in CD34+, HLA-DR+ cells. These treatments were associated with > or = 50% inhibition of the assayable CFU-GEMM colony numbers. Incubation in serum-free medium (SFM) alone for 24 h also induced apoptosis of CD34+, HLA-DR+ cells, which was associated with reduced intracellular levels of the bcl-2 gene product p26BCL-2. Co-treatment with pIXY321 (10 ng/ml) inhibited apoptosis of CD34+, HLA-DR+ cells incubated in SFM, without significantly increasing the intracellular p26BCL-2 levels. Furthermore, co-treatment with pIXY321 significantly reduced taxol- and Ara-C-induced apoptosis and promoted the survival of CFU-GEMM (P < 0.05). Taxol and Ara-C mediated apoptosis of CD34+, HLA-DR+ cells, and its inhibition by pIXY321, was not accompanied by any significant alteration in the intracellular p26BCL-2 levels. By demonstrating that co-treatment with pIXY321 confers significant protection against apoptosis of CD34+, HLA-DR+ cells as well as promotes survival of normal HPC exposed to clinically relevant schedules and concentrations of taxol of Ara-C, these results support the design of chemotherapy regimens incorporating pIXY321 plus taxol and/or high-dose Ara-C for solid tumors and/or acute leukemias. It is hoped that the use of such a cytokine might maintain normal HPC numbers following chemotherapy, therefore avoiding prolonged suppression.

Antigens, CD34↗
PubMed1995

[Some biochemical indexes in white rabbit's blood affected by acute high intensity microwave].

Irradiation of white rabbits by 10, 50, 100 and 200 mW/cm2 microwave respectively can cause the disorder of protein metabolism, the abnormality of blood sugar, and the change of the activity of serum alpha-hydroxybutyrate dehydrogenase, lactate dehydrogenase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase, acid phosphatase ect. These changes can be used as indexes in the evaluation of the effect of acute high intensity microwave exposure. The effect on the organism mainly depends on the intensity of exposure provided the dose of microwave remains the same.

Acid Phosphatase↗
PubMed1995

Localization and quantification of cholecystokinin receptors in rat brain with storage phosphor autoradiography.

The present study evaluated a new imaging technique that demonstrated the application of storage phosphor autoradiography in the localization and quantification of cholecystokinin receptors in rat brains and compared the results with film autoradiography. Cryostat sections were incubated with [125I]Bolton-Hunter-labeled sulfated cholecystokinin octapeptide followed by exposure to a storage phosphor-imaging screen and suitable autoradiography film. To obtain satisfactory images, it took 6 days with film autoradiography vs. 15 hours with the storage phosphor technique. Both film and storage phosphor autoradiograms showed the same cholecystokinin receptor distribution in brain sections; however, the film imaged more details. To reach the lowest possible response ratio between low and high receptor density regions in rat brains, storage phosphor autoradiography was about 240-fold faster than film. In addition, the new technique presented a considerably larger exposure time range for maintaining that ratio. The binding per area showed a linear relationship with the thickness of sections between 5 and 14 microns. In the linear response range, the quantitative results of both methods are comparable. In conclusion, storage phosphor autoradiography is a faster technique for localizing and quantifying peptide receptors in tissue sections but slightly compromised in resolution when compared with film autoradiography.

Animals↗
PubMed1994

Structure of the gamma subunit of Escherichia coli F1 ATPase probed in trypsin digestion and biotin-avidin binding studies.

The arrangement and functional role of the gamma subunit of the Escherichia coli F1ATPase (ECF1) has been probed by protease digestion and avidin-biotin labeling experiments using wild-type enzyme and four mutants, gamma S8C, gamma T106C, gamma S179C, and gamma V286C, respectively. Trypsin was found to cleave the gamma subunit at four sites, Arg70, Lys199, Lys201, and Lys212. Cleavage at these four sites did not greatly reduce the high ATPase activity of the enzyme that is obtained when the epsilon subunit is removed by the protease treatment. However, prolonged trypsin cleavage led to loss of inhibition by epsilon subunit added back to the trypsin-treated enzyme. Endoproteinase-Lys-C cleaves the gamma subunit of ECF1 at three of the four sites, i.e. Lys199, Lys201, and Lys212, but not at Arg70. The enzyme was activated by treatment with this protease because of degradation and release of the epsilon subunit, but added pure epsilon subunit still caused inhibition of ATPase activity. Therefore, cleavage at Arg70 by trypsin is responsible for the loss of response to the epsilon subunit inhibition. Biotin was reacted with Cys residues at positions 8, 106, 179, and 286 in different gamma subunit mutants and the accessibility of the biotin to avidin monitored in the intact ECF1 from the different mutants. Avidin was able to react with biotin when incorporated at position 106, not at 8, 179, or 286. The four trypsin cleavage sites, Arg70, Lys199, Lys201, and Lys212, as well as Thr106 are in regions of the gamma subunit predicted to be mainly beta-sheet and beta-turn structures.

Amino Acid Sequence↗
PubMed1994

Contrast dependence of colour and luminance motion mechanisms in human vision.

Conventional views of visual perception propose a colour-blind pathway conveying motion information and a motion-blind pathway carrying colour information. Recent studies show that motion perception is not always colour blind, is partially dependent on attention, can show considerable perceptual slowing around isoluminance and is contrast-dependent. If there is a single motion pathway, receiving luminance and chromatic input, then the dependence of relative perceived velocity on relative stimulus contrast should be the same for both luminance and chromatic targets. Here we provide a distinctive characterization of the motion mechanisms using a robust velocity-matching task. A relative contrast scale allows direct comparison of the performance with luminance and chromatic targets. The results show that the perceived speed of slowly moving coloured targets at isoluminance has a steep contrast dependence. The perceived speed of slowly moving luminance targets shows a much lower contrast dependence. At high speeds the contrast dependence is low for both luminance and isoluminant stimuli, although the behaviour is unlike either of the slow mechanisms. The results suggest two independent pathways that perceive slowly moving targets: one is luminance-sensitive and the other is colour-sensitive. Fast movement is signalled via a single motion pathway that is contrast-invariant and not colour blind.

Color Perception↗
PubMed1994

Regression of collagen-induced arthritis with taxol, a microtubule stabilizer.

OBJECTIVE: To investigate the capacity of taxol, a microtubule stabilizer, to inhibit collagen-induced arthritis (CIA), a model of rheumatoid arthritis. METHODS: Louvain rats were immunized with type II collagen (day 0) to induce arthritis. Taxol was administered beginning on day 2 (prevention protocol) or at arthritis onset on day 9 (in either a high-dose or low-dose suppression protocol). Rats were assessed clinically and radiographically for arthritis severity. Cellular and humoral immune responses to type II collagen were also evaluated. RESULTS: Institution of taxol prior to arthritis onset completely precluded the development of CIA (P < 0.0001 versus controls). It also suppressed established clinical disease (high-dose protocol P < 0.0000001; low-dose protocol P < 0.0001) and radiographic erosions (high-dose protocol P < 0.00001; low-dose protocol P < 0.001) compared with controls. Levels of IgG antibodies, but not delayed-type hypersensitivity, to type II collagen were reduced after taxol administration. CONCLUSION: Taxol completely prevented the induction of CIA and caused significant regression of existing arthritis.

Animals↗
PubMed1994

1-beta-D-arabinofuranosylcytosine-, mitoxantrone-, and paclitaxel-induced apoptosis in HL-60 cells: improved method for detection of internucleosomal DNA fragmentation.

We investigated the ability of different doses and durations of exposure to the chemotherapeutic drugs 1-beta-D-arabinofuranosylcytosine (Ara-C), mitoxantrone (MTN), and paclitaxel (taxol, TXL) to induce internucleosomal DNA fragmentation and apoptosis in human acute myeloid leukemia (AML) HL-60 cells in suspension culture. At clinically achievable concentrations, all three drugs have been shown to induce apoptosis in HL-60 cells. An improved method was developed for the isolation of pure genomic DNA and the detection of drug-induced internucleosomal DNA fragmentation in < 1.0 microgram of DNA sample by agarose gel electrophoresis. Morphologic evidence for apoptosis was determined by light microscopy following Wright staining, and cell viability was assessed by trypan blue dye exclusion. Internucleosomal DNA fragmentation was observed following exposure to 1.0 microM Ara-C for 4 h, which increased with 10 and 50 microM Ara-C. Incubation with 100 microM Ara-C produced internucleosomal DNA fragmentation starting at 3 h, which increased with longer periods of exposure to Ara-C. Utilizing a schedule of 1-h exposure followed by 3-h suspension in drug-free medium, 0.25 microM MTN was found to initiate DNA fragmentation, which increased with exposure to 1.0 and 5.0 microM MTN. However, identical treatment with higher concentrations of MTN resulted in random DNA degradation. Alternatively, continuous exposure to 1.0 microM MTN for 3 h was necessary to initiate internucleosomal DNA fragmentation. This increased with exposure intervals of up to 6 h. Exposure to TXL concentrations as low as 0.01 microM for 24 h caused internucleosomal DNA fragmentation, which increased with dose escalation (0.05, 0.1, 0.5, and 1.0 microM) of TXL. Although continuous exposure to 1.0 microM TXL for a period as short as 8 h produced internucleosomal DNA fragmentation, this increased significantly with longer exposure intervals. In general there appears to be a threshold concentration and duration of exposure below which none of these three drugs activates endonucleolytic internucleosomal DNA fragmentation and apoptosis. This threshold is lower for the DNA-interactive drugs MTN and Ara-C but higher for the non-DNA-interactive drug TXL. Higher doses or prolonged treatments with the drugs produce random DNA fragmentation associated with necrotic cell death. These in vitro results may further improve our understanding of the antileukemic cytotoxic effects of these drugs, which may enable a more rational design of drug regimens for optimal treatment of AML.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Combined antileukemic activity of pIXY 321 and Ara-C against human acute myeloid leukemia cells.

Prolonged administration of conventional (100 mg/m2/day) or low dose Ara-C (20 mg/m2/day) has been associated with significant clinical antileukemic effects in AML and myelodysplastic syndromes. These doses and schedules of Ara-C yield plasma Ara-C concentrations in the range of 10 to 100 nM. Utilizing concentrations and a schedule of Ara-C treatment, representative of Ara-C exposures in these clinical situations, we performed in vitro studies to examine the effects of co-treatment with pIXY 321 on Ara-C induced apoptosis and Ara-C-mediated colony growth inhibition of human myeloid leukemia HL-60 cells. Significantly greater internucleosomal DNA fragmentation, higher percentage of morphologically recognizable apoptotic cells and increased colony growth inhibition were observed following treatment with 100 versus 10 nM Ara-C for 5 days. Simultaneous exposure to 10 ng/ml pIXY 321 resulted in significantly increased colony growth inhibition as well as DNA fragmentation and apoptosis due to 10 nM but not 100 nM Ara-C. These concentrations of Ara-C inhibited c-myc and did not induce c-jun mRNA expression. These effects of Ara-C on c-myc and c-jun expressions were not influenced by co-treatment with pIXY 321. Neither treatment with pIXY 321 or Ara-C alone, nor co-treatment with pIXY 321 and Ara-C, significantly altered the intracellular p26BCL-2 levels in HL-60 cells. These results indicate that co-treatment with pIXY 321 significantly increases low dose Ara-C-induced apoptosis and thereby its antileukemic activity.

Acute Disease↗
PubMed1994

High levels of p26BCL-2 oncoprotein retard taxol-induced apoptosis in human pre-B leukemia cells.

In human leukemic cells clinically relevant concentrations of taxol have been demonstrated to induce the biochemical and morphologic hallmarks of apoptosis (Leukemia 1993;7:563-568). Since overexpression of the bcl-2 gene has been reported to retard apoptosis due to a variety of anticancer agents, we examined and compared taxol-induced intracellular microtubular bundling and apoptosis in pre-B human leukemia 697 cells and their counterparts which have been transfected with and overexpress cDNA derived from the bcl-2 gene. Treatment with 0.1 or 1.0 mumol/l taxol for 24 h resulted in internucleosomal DNA fragmentation and morphologic features of apoptosis in 697 cells, but not in 697/BCL-2 cells. However, indirect immunofluorescent staining with anti-tubulin antibody revealed that taxol treatment produces stable microtubule bundles resistant to calcium-mediated disassembly in 697, as well as 697/BCL-2 cells. In addition, taxol-induced microtubule bundling was associated with a marked accumulation of the two cell types in the G2/M phase of the cell cycle. Following exposure to taxol, when 697 cells were washed and kept in drug-free medium, they showed rapid onset of apoptosis followed by loss of cell viability and a decline in cell numbers. In contrast, identically treated 697/BCL-2 cells kept in drug-free medium remained in a growth arrested state, but showed little evidence of apoptosis for up to 4 days. They eventually demonstrated features of apoptotic cell death and loss of viability between 5 and 7 days. This was not accompanied by a decrease in p26BCL-2 levels. Anti-phosphotyrosine or anti-MAP kinase immunoblot analyses of proteins isolated from taxol-treated 697 and 697/BCL-2 cells failed to show any difference in tyrosine phosphorylation of cellular proteins. Therefore, our findings indicate that in 697/BCL-2 cells, high levels of p26BCL-2 significantly delay taxol-induced endonucleolytic internucleosomal DNA fragmentation and apoptosis, but do not affect taxol-induced microtubule bundling or cell cycle growth arrest. The delayed onset of taxol-induced DNA fragmentation and apoptosis in 697/BCL-2 cells without down-regulation of p26BCL-2 levels suggests that an alternative mechanism of taxol-mediated apoptosis might be triggered which is unimpeded by high p26BCL-2 levels, or taxol-induced prolongation of mitotic arrest may lead to the inactivation or inhibition of that mechanism by which p26BCL-2 is able to block apoptosis.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

Characterization of a human myeloid leukemia cell line highly resistant to taxol.

Taxol-resistant sublines of HL-60 myeloid leukemia cells (HL-60/TAX100 and HL-60/TAX1000) have been isolated in vitro by subculturing in progressively higher concentrations of taxol. HL-60/TAX100 and HL-60/TAX1000 cells are capable of continuous growth in the presence of 0.1 microM and 1.0 microM taxol, respectively, and the IC50 (50% growth inhibitory dose) values for taxol for the two sublines are 0.34 and 2.44 microM as compared to 3.1 nM for the parent HL-60 cells. HL-60/TAX100 and HL-60/TAX1000 cells display a variable degree of cross-resistance to taxotere, vincristine and doxorubicin, but are sensitive to the antimetabolite Ara-C. Both HL-60/TAX100 and HL-60/TAX1000 cells over-express MDR-1 m-RNA and the membrane efflux multidrug transporter P-glycoprotein (PGP), as determined by Western blot and immunofluorescence labeling with anti-PGP antibodies. Consequently, exposure of the taxol-resistant cells to [3H]taxol or daunomycin results in the accumulation of significantly lower levels of the two drugs. Co-treatment with cyclosporine (0.5 microgram/ml) or verapamil (10 microM) partially overcomes taxol resistance in HL-60/TAX1000 cells. Following treatment with clinically relevant concentration of taxol (1.0 microM for 24 h), HL-60 but not HL-60/TAX1000 cells display intracellular microtubular bundling, markedly enhanced accumulation of the cells in G2/M phase of cell-cycle and internucleosomal DNA fragmentation associated with apoptosis which is independent of bcl-2 gene expression. These taxol-resistant myeloid leukemia cells may serve as in vitro experimental models for examinating strategies which may have potential applicability for overcoming taxol resistance.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1994

[Ultrastructural change of brain ganglion of Oncomelania hupensis after immersion in sodium pentachlorophenate].

The ultrastructure of the fibrous sheath, the layer of ganglionic cell bodies and the neuropil of brain ganglion of Oncomelania hupensis was first observed under transmission electron microscope. Ultrastructural changes were found in the brain ganglion after immersing the snails in sodium pentachlorophenate. The mitochondria of nerve fibers and neurons showed denaturation and necrosis, and glycogen in neurones was markedly reduced; the neuropil also exhibited denaturation and necrosis. The ultrastructural findings may explicate in some way the mechanism of molluscicidal action of NaPcP on Oncomelania hupensis via its action on the nervous system (Figs. 1-6).

Animals↗
PubMed1994

Clozapine effects on glucose metabolic rate in striatum and frontal cortex.

Eighteen patients with schizophrenia had cerebral metabolic rates assessed with positron emission tomography during a double-blind, placebo-controlled crossover study of clozapine treatment. Relative metabolic rates were increased in the basal ganglia, especially on the right side. In the frontal lobe, metabolic rates were lowered, more on the left than on the right. The anterior nuclei of the thalamus also showed lower metabolic rates after clozapine. We have previously observed patients with schizophrenia to have low metabolic rates in the basal ganglia and to lack the normal right > left asymmetry; in this study, clozapine normalized striatal activity. In the frontal lobe, asymmetry was normalized, but hypofrontal function was, if anything, exaggerated. This effect in the frontal lobe was not observed with haloperidol in earlier studies. The cortical effects of clozapine may be related to its unique clinical properties and suggest important differences between typical and atypical antipsychotic drugs.

Adult↗
PubMed1993

Tissue distribution of cytochrome c oxidase isoforms in mammals. Characterization with monoclonal and polyclonal antibodies.

Monoclonal and polyclonal antibodies specific to the two isoforms of subunit VIa of bovine cytochrome c oxidase were generated and used to study the tissue distribution of this subunit pair in beef, human and rat. The so-called H-(heart) form was found exclusively in heart and skeletal muscle, whereas the so-called L-(liver) form was the only isoform present in brain, kidney, liver and smooth muscle. Little or no L-form was detected in skeletal muscle. In bovine heart no subunit VIa-L was detected, while in human heart the subunit VIa-H and VIa-L isoforms were present in roughly equal proportions. These results imply that, in humans, the deficiency of a subunit VIa isoform may have a different effect on the physiology of heart then on the physiology of skeletal muscle.

Amino Acid Sequence↗
PubMed1993

High-dose mitoxantrone induces programmed cell death or apoptosis in human myeloid leukemia cells.

Mitoxantrone has been shown in vitro to exhibit a steep dose-response relationship with respect to the clonogenic survival of acute myeloid leukemia cells. In this report, we show that 1-hour exposure of human myeloid leukemia HL-60 and KG-1 cells to mitoxantrone concentrations ranging between 0.1 and 10.0 mumol/L induced internucleosomal DNA fragmentation of approximately 200-bp integer multiples, characteristic of cells undergoing programmed cell death (PCD) or apoptosis. Mitoxantrone-mediated PCD was associated with a steep inhibition of the clonogenic survival of the leukemic cells. In addition, intracellularly, mitoxantrone-induced PCD was associated with a marked induction of c-jun and significant repression of c-myc and BCL-2 oncogenes. Pretreatment with the protein kinase C stimulator phorbol myristate acetate enhanced mitoxantrone-induced internucleosomal DNA fragmentation, whereas protein kinase C inhibitors staurosporine and H7 had no effect. These findings suggest that PCD is a potential mechanism underlying the steep dose-response relationship of mitoxantrone to the inhibition of clonogenic survival of acute myeloid leukemia cells.

Apoptosis↗